Pain

The International Association for the Study of Pain (IASP) defines pain as:

'An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in such terms.' (1)

This definition is important to understand, because it breaks with a simple 'injury = pain' logic.

1.1 Pain is an experience, not necessarily tissue damage

• Pain is subjective – there is no 'pain test' or objective measurement.
• Pain is both sensory (intensity, location, quality) and emotional (fear, sadness, frustration).
• Pain can occur without tissue damage, and tissue damage can be present without pain.

1.2 Pain and the brain

The brain interprets and constructs the pain experience based on (1):

• sensory input (nociception)
• previous experiences
• expectations
• emotional state
• context (situation, safety, information)

1.3 Pain categories

• Nociceptive pain – tissue damage, inflammation
• Neuropathic pain – damage in the nervous system
• Visceral pain – internal organs
• Somatic pain – skin, muscles, skeleton
• Sclerotomic pain – deep supportive tissue
• Myotomic pain – musculature
• Centralized pain – persistent pain due to changes in the CNS (4)

2.1 Acute pain

Acute pain is a warning signal.(4) that:

• warns of injury or threat
• activates the sympathetic nervous system
• increases heart rate, blood pressure, pupil dilation, cold sweat
• triggers protective behavior

2.2 Chronic pain

Chronic pain (often defined as > 3 months) is characterized by the fact that it:

• loses its biological function as a warning signal
• often gives few or no autonomic signs
• is often not directly linked to ongoing tissue damage
• is strongly influenced by psychology and social context
• is associated with depression, anxiety, sleep disturbances, inactivity, and social isolation (4)

Chronic pain can be understood as a form of "learned" or "plastic" state in the nervous system – where pain pathways have become hypersensitive, and the brain has "learned" pain.

3.1 Grading of Acute Pain

• Acute pain is usually graded according to intensity, because the goal is to assess severity and effect of treatment.
• The most commonly used tools are the Numerical Rating Scale (NRS) and Visual Analog Scale (VAS), which measure pain on a scale from 0–10. This provides a quick measure of how strong the pain is and is used to monitor response to treatment over time.
• Acute pain tools focus primarily on pain intensity and the degree of relief after interventions.

Tools:

• VAS (Visual Analogue Scale)
• NRS (Numeric Rating Scale)
• VRS (Verbal Rating Scale)

VAS and NRS are more sensitive than VRS for small changes.

3.2 Grading of chronic pain

Chronic pain is graded more broadly than acute pain, because intensity alone does not describe the disease burden. Often, the Chronic Pain Grade Scale (CPGS) is used, which assesses both:

• Pain intensity
• Functional impairment
• How much the pain affects work, activity, and social participation

The scale classifies patients into five grades (0–IV) from no pain to high functional impairment and severely restricted lifestyle. Chronic pain tools also include assessment of psychological factors, coping, and quality of life, because these are central in long-term pain conditions.

Chronic pain must therefore be assessed in light of:

• function
• emotions
• sleep
• social participation
• work ability
• quality of life

A good pain history is one of the doctor's most important tools.

4.1 Pain history

Ask systematically about:

• location
• spread
• intensity
• quality
• onset
• duration
• aggravating factors
• relieving factors

4.2 Impact on function and life

Ask specifically about:

• sleep
• physical function
• work ability
• finances
• family life
• social life
• sexual function

4.3 Psychosocial factors

Also ask about:

• symptoms of depression
• anxiety
• concern about serious illness
• insurance matters
• previous traumas
• coping strategies

The MPQ maps how how the pain is experienced, not just how painful it is (3).

5.1 What the MPQ measures

• Sensory qualities – stabbing, burning, aching, gnawing, etc.
• Affective qualities – exhausting, frightening, nauseating, painful
• Intensity – VAS and categorical scale (3)

5.2 Why MPQ is clinically useful

Pain quality often provides better information about cause than intensity alone (3).

Examples:

• Burning, stabbing, electric → neuropathic pain
• Deep, aching, toothache-like → sclerotomal pain
• Pressing, bursting → muscular, vascular, or visceral
• Exhausting, nauseating → high affective component

5.3 Structure in NSF-MPQ

NSF‑MPQ stands for the Norwegian Short‑Form McGill Pain Questionnaire. It is a validated, multidimensional questionnaire used to assess the quality and intensity of a patient's pain (5).

• Sensory adjectives (e.g., throbbing, stabbing, aching)
• Affective adjectives (e.g., tiring, nauseating, frightening)
• VAS scale (0–100 mm) for pain intensity
• Current pain level (0–5)

5.4 Interpretation

• High sensory score → strong nociceptive/neuropathic component
• High affective score → significant emotional burden
• High total score → substantial pain experience

5.5 Clinical examples

• Burning + electric → neuropathy
• Deep + aching → sclerotome
• Exhausting + frightening → central sensitization

Pain is influenced by biological, psychological, and social factors. (1)

6.1 Biological factors

• nociception
• neuropathy
• central sensitization
• genetics
• sleep disturbances

6.2 Psychological factors

• anxiety
• depression
• catastrophic thinking
• coping strategies
• expectations

6.3 Social factors

• work situation
• family
• finances
• culture
• sick role

The FABQ model is based on the Fear-Avoidance Model of Pain, developed to explain why some people with acute pain recover, while others develop long-term pain and loss of function. The model was founded by Waddell and colleagues in 1993 and forms the basis for the FABQ questionnaire. FABQ measures patient's fear of pain, movement, and work. (2) Patients interpret pain differently. Some see pain as harmless → remain active → get better. Others catastrophize pain → develop fear of movement and avoidance behavior with subsequent reduced activity → more pain, impaired function, depression, and an increased risk of chronicity.

7.1 Theoretical background – The Fear-Avoidance Model

The model thus describes how fear and avoidance can lead to chronic pain. Two main pathways after a pain episode (6):

A) Avoidance (maladaptive response)

• pain is interpreted as danger
• movement is avoided
• inactivity → more pain, stiffness, weakness
• increased fear
• risk of depression and disability

B) Confrontation (adaptive response)

• the patient understands that pain ≠ injury
• activity resumes
• mastery increases
• function improves

7.2 FABQ scales

FABQ-Physical activity (scored from 0–24)

High score ≥ 16 → significant fear of movement

FABQ-Job (scored from 0–42)

High score ≥ 25 → high risk of sick leave and poor prognosis regarding disability. (2, 6)

7.3 Clinical significance

High FAB (Fear‑Avoidance Beliefs) describes the beliefs a person has that physical activity or work will worsen pain or injury and is associated with:

• chronic pain
• central sensitization
• sick leave
• poor treatment response
• passive coping

7.4 Three types of avoidance behavior toward physical activity and work and possible treatment measures

1. Misinformation and uncertainty
   • Treatment: reassurance, information and graded activity
2. Learned avoidance
   • Treatment: graded exposure, functional training
3. Affective avoidance/phobia
   • Treatment: cognitive therapy, exposure, work with catastrophic thoughts

7.5 Clinical examples

• FABQ-Physical activity = 20 → fear of movement
• FABQ-Work = 32 → high risk of long-term sick leave

Early in fetal development the body is divided into somites – segmented blocks of mesoderm. (4)

The somites form:

• Dermatome → skin
• Myotome → musculature
• Sclerotome → skeletal structures

The sclerotome forms:

• vertebral body
• vertebral arch
• intervertebral structures
• deep ligaments
• periosteum
• joint capsules

Sclerotomal pain is deep somatic pain from structures such as (4):

• facet joints
• SI joint
• ligaments
• periosteum
• outer annulus fibrosus

9.1 Characteristics of pain

• deep, dull, toothache-like
• diffuse distribution
• the patient often points with the whole hand
• referred pain
• normal sensation
• normal strength

Characterized by sharp, electric, burning pain in a dermatome, often with neurological deficits. (4)

10.1 Characteristics of pain

• sharp
• electric
• burning
• follows a dermatome
• worsens with cough/sneeze/Valsalva
• paresthesias
• sensory deficits
• reflex deficits
• motor deficits

Myotomal pain originates from muscles and muscle-related structures. Deep, aching pain that worsens with muscle use and is relieved by rest. (4)

11.1 Characteristics of pain

• deep, aching pain
• worsens with muscle use
• relieved by rest
• can give a feeling of stiffness
• normal skin sensitivity
• normal reflex status
• segmental weakness may occur with severe irritation

11.2 Typical sources of pain

• muscle tension
• myofascial trigger points
• muscle injuries
• overuse
• static work

Rexed's lamina V in the spinal cord contains wide dynamic range neurons (WDR). (4)

These neurons receive signals from:

• cutaneous nociceptive fibers
• muscular fibers
• joint fibers
• visceral fibers

This phenomenon is called convergence. WDR neurons in the spinal cord receive signals from many different types of peripheral nerves simultaneously – both A‑beta, A‑delta, and C fibers. This convergence allows a single spinal cord neuron to integrate information from multiple tissue types and large areas of skin.

12.1 Clinical significance

Convergence explains:

• referred pain
• why pain from deep structures is experienced as diffuse
• why visceral pain can be experienced as somatic
• why patients often point with the whole hand

Referred pain means that the pain is experienced in another location than where it originates (4).

13.1 Characteristics of pain

• diffuse
• deep
• difficult to localize
• does not follow dermatomes
• normal sensation
• normal strength

13.2 Examples of pain distribution

• Facet joints → shoulder blade, thoracic
• SI joint → buttock, back of thigh
• Diaphragm → shoulder
• Heart → left arm, jaw

Central sensitization involves increased sensitivity in the CNS (4). When the nervous system is bombarded with persistent nociceptive signals, the spinal cord and brain begin to "turn up the volume" on pain. Neurons that previously required strong stimulation start firing with weak or normal touch. The brain also expands its map, so pain is experienced over larger areas than where the problem actually is. The result is a nervous system that reacts too strongly, for too long, and to too much – even when the tissue damage is minimal or gone. Over time, pain can "teach itself," because the nervous system changes connections and strengthens pathways that convey pain. This means that the pain can be maintained by the network itself – not from an ongoing injury. The brain becomes better at producing pain than at dampening it, much like a learned pattern. Therefore, the patient can have real, intense pain even if all tissue findings are normal – because the pain is now a product of neuroplastic changes.

14.1 Characteristics of pain

• pain from light stimuli (allodynia)
• increased pain from normal stimuli (hyperalgesia)
• widespread pain
• fatigue
• sleep disturbances
• cognitive difficulties ("brain fog")

14.2 Conditions associated with central sensitization and neuroplastic pain

• fibromyalgia
• chronic fatigue syndrome
• irritable bowel
• chronic headache
• long-term MSK complaints

Pain occurs in the brain, and therefore it is affected by thoughts, emotions, expectations, and past experiences. When we are afraid, stressed, or worried, the brain increases sensitivity – like turning up the volume on a sound system. Positive expectations, security, and understanding can, on the other hand, reduce pain signals and make the nervous system less reactive. Psychology is therefore not about pain being 'imagined', but about how the brain modulates real, physiological pain.

Pain is affected by:

• thoughts
• emotions
• expectations
• previous experiences
• coping strategies

15.1 Catastrophic thinking

Catastrophizing means that the brain interprets pain as more dangerous than it is and creates 'worst-case scenarios.' This leads to more fear, more attention to pain, and a stronger pain experience. The body goes into alarm mode, and the nervous system increases sensitivity. The result is a self-reinforcing circle where thoughts make the pain greater than the tissue signal itself would suggest.

Catastrophizing (6) is a strong predictor of:

• pain intensity
• functional loss
• sick leave
• poor treatment response

15.2 Depression and anxiety

Pain and depression/anxiety are closely linked because the brain uses the same networks to regulate both emotions and pain. When a person is depressed or anxious, the body's stress and alarm system becomes more active, and pain signals are amplified. At the same time, the brain's own pain-relieving mechanisms are weakened, so that even small signals can be experienced as strong. The result is that pain, depression, and anxiety often reinforce each other in a self-sustaining loop.

Long-term pain affects:

• pain perception
• motivation
• sleep
• activity

Pain and sleep affect each other in both directions. When you sleep poorly, the brain becomes more sensitive and the pain system is more easily activated. At the same time, pain makes it more difficult to fall asleep and maintain deep sleep, so the body gets less time to repair and regulate. The result is a vicious cycle where little sleep causes more pain, and more pain leads to poorer sleep.

Lack of sleep increases pain sensitivity and the risk of chronic pain development. Sleep and pain affect each other mutually. (4)

16.1 Lack of sleep causes:

• increased pain sensitivity
• reduced pain tolerance
• increased risk of chronification

16.2 Pain causes:

• difficulties falling asleep
• frequent awakenings
• reduced deep sleep

Pain and work strongly affect each other. When people are working, they stay active, have structure, and experience mastery – which often reduces pain and improves function. Long-term absence, on the other hand, can increase focus on pain, reduce capacity, and make the return path harder. Therefore, adapted work is often one of the most effective "treatments" for musculoskeletal pain.

Work can both protect against and worsen pain, depending on demands, control, and support (6):

• protect against pain
• worsen pain
• be part of the solution
• be part of the problem

17.1 Work as treatment

Work provides:

• structure
• social contact
• mastery
• physical activity
• financial security

17.2 Work as a burden

Work can worsen pain by:

• high demands
• low control
• poor support
• heavy lifting
• static work

Clinical assessment of pain involves integrating the patient's symptoms, function, psychosocial factors, and clinical findings into a holistic understanding of what drives the pain. The goal is not only to find a diagnosis but to identify mechanisms – nociceptive, neuropathic, nociplastic, and psychosocial influences. The assessment guides the choice of interventions, prognosis, and the need for further investigation. This is a dynamic process that is updated as new information emerges.

Clinical assessment of pain requires evaluation of pain category, function, and psychosocial factors and is about (4):

• understanding the patient's pain
• identifying the pain category
• assessing function
• assessing psychosocial factors
• making a plan that the patient understands and believes in

18.1 Important questions

• What does the patient believe?
• What does the patient fear?
• What does the patient avoid?
• What does the patient want to achieve?

Effective treatment of pain is active, function-oriented, and mastery-based. This means that the patient should do something, not just have something done to them. The measures are aimed at restoring function in everyday life, not just reducing symptoms. The patient must learn strategies that provide control, security, and increased capacity over time. The goal is lasting improvement through activity, adaptation, and self-management – not passive treatment. Effective treatment is active, function-oriented, and mastery-based (4).

19.1 Principles in treatment

• reassurance
• activity
• graded exposure
• mastery
• sleep
• stress reduction
• interdisciplinarity

19.2 What works poorly?

• passive treatment alone
• overdiagnosis
• unnecessary imaging diagnostics
• unnecessary surgery
• prolonged sick leave

1. Pain is a complex biopsychosocial experience that requires holistic assessment and treatment.
2. Acute and chronic pain are fundamentally different.
3. Pain quality (MPQ) provides important diagnostic information.
4. Fear and avoidance (FABQ) drive chronification.
5. Sclerotome, myotome, and dermatome produce different pain patterns.
6. Central sensitization is common in long-lasting complaints.
7. Psychology, sleep, and work strongly influence pain.
8. Treatment must be active, function-oriented, and mastery-based.

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